research suggests Crohn’s scarring
London — Research suggests scientists have identified what drives the development of scar tissue in the intestines of people with Crohn’s disease.
Scientists found clusters of immune cells in the gut which may be stimulating nearby cells to generate excess scar tissue, known as fibrosis.
It is hoped the discovery, detailed in a new study, could help develop treatments to prevent or slow the development of fibrosis, a serious complication of Crohn’s disease.
Crohn’s is a long-term, inflammatory condition affecting the digestive tract and, over time, ongoing inflammation can lead to fibrosis, where excess collagen builds up in the bowel wall.
This scarring can cause the intestine to narrow and become blocked, meaning that surgery is needed.
The University of Edinburgh-led research team hope the latest findings could help pinpoint therapeutic targets that could be explored to interrupt the scarring process and develop treatments specifically aimed at fibrosis.
Shahida Din, consultant gastroenterologist at NHS Lothian and honorary senior clinical lecturer at the University of Edinburgh, said: “Fibrosis remains one of the most challenging complications of Crohn’s disease because current treatments primarily target inflammation rather than the scarring itself.”
research suggests Crohn’s scarring
“Understanding the cellular signalling pathways that link immune activity to collagen production could help guide the development of therapies aimed at preventing or slowing fibrosis.”
The research team analysed intestinal tissue samples from Crohn’s disease patients with fibrosis, focusing on the ileum – the final part of the small intestine where the disease most commonly develops.
The researchers used archived intestinal tissue samples to examine structural changes across the different layers of the bowel wall.
They found significantly increased fibrosis and immune cell infiltration in Crohn’s disease tissue compared with normal tissue.
The submucosa – a deeper layer of the bowel wall – had particularly high levels of scarring, indicating it may play an important role in the early stages of fibrosis.
Researchers next analysed fresh intestinal tissue samples using a cutting-edge technique to study gene activity in individual cells, known as single-cell RNA sequencing.
They identified a link between clusters of immune cells, known as Crohn’s lymphoid aggregates, and groups of endothelial cells, which normally line blood vessels.
Scientists found that the endothelial cells appeared to form distinctive structures surrounding the Crohn’s lymphoid aggregates.
Further analysis revealed signalling interactions between these clusters and nearby cells responsible for producing collagen, suggesting they may actively promote fibrosis.
research suggests Crohn’s scarring
Michael Glinka, research fellow at the University of Edinburgh, said: “Our findings highlight previously unrecognised interactions between immune cells, endothelial cells and collagen-producing cells in Crohn’s disease.”
“By combining traditional pathology with single-cell transcriptomics, we were able to confirm these changes using two independent approaches and uncover biological signalling pathways that may provide new therapeutic targets.”
The research is published in The Journal of Pathology.
It was conducted by a UK-wide collaboration of researchers and clinicians and was supported by funding from the Leona M and Harry B Helmsley Charitable Trust.
Catherine Winsor, director of service, research and evidence at the charity Crohn’s & Colitis UK, said: “People who live with Crohn’s often tell us how much fibrosis and scarring can affect their lives, yet it’s something current treatments don’t address.”
“This early research is really exciting because it helps us to understand what drives that scarring and where new treatments could make a difference.”
“It brings real hope that, in the future, we might be able to treat not just inflammation, but the lasting damage Crohn’s can cause.”
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